Gene Ontology annotation through association of InterPro records with GO terms
Annotation inferences using phylogenetic trees
Electronic Gene Ontology annotations created by ARBA machine learning models
Regulation of transcription at the Saccharomyces cerevisiae start transition by Stb1, a Swi6-binding protein.
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Cln1-Cdc28 kinase complexes immunoprecipitated from yeast phosphorylate recombinant Stb1 more efficiently than histone H1, and the in vivo Stb1 phosphoforms are assigned to Cln1/Cln2-Cdc28 rather than Cln3-Cdc28.
"Stb1 was an excellent substrate for both the Cln1-Cdc28 and Cln2-Cdc28 kinases in vitro and was a better in vitro substrate than histone H1"
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CLN1 transcription at Start is driven by SBF (Swi4-Swi6) acting through MCB elements.
"CLN1 transcription is regulated through MCB elements that are dependent upon SBF (Swi4/Swi6)"
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Cln1 and Cln2 are dispensable for activating Start transcription but required for executing the downstream Start events of budding and DNA synthesis.
"CLN1 and CLN2 are not required for gene activation but are important for the proper execution of other Start-related events such as budding and DNA synthesis"
A comprehensive analysis of protein-protein interactions in Saccharomyces cerevisiae.
Nuclear-specific degradation of Far1 is controlled by the localization of the F-box protein Cdc4.
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Cln1-GFP and Cln2-GFP are both distributed between the nucleus and the cytoplasm.
"Cln1–GFP as well as Cln2–GFP were localized in both the nucleus and the cytoplasm"
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Ubiquitylation of the G1 cyclins Cln1 and Cln2 is mediated by SCF(Grr1) rather than SCF(Cdc4) - a background statement in this paper, not one of its own experiments.
"ubiquitylation of the G 1 cyclins, Cln1 and Cln2, and the bud emergence protein Gic2 is mediated by SCF Grr1"
Functional organization of the yeast proteome by systematic analysis of protein complexes.
Systematic identification of protein complexes in Saccharomyces cerevisiae by mass spectrometry.
Late-G1 cyclin-CDK activity is essential for control of cell morphogenesis in budding yeast.
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The late-G1 burst of cyclin-CDK activity contributed by CLN1,2 and PCL1,2 is required for cell morphogenesis - septin ring assembly and Cdc24 localisation at the bud site - but not for DNA replication.
"a build-up or burst of G1
cyclin-dependent kinase (CDK) activity through activation of the cyclin genes
CLN1,2 and PCL1,2 is essential for cell morphogenesis, but not for other events
associated with the G1-S-phase transition, including DNA replication."
Assigning function to yeast proteins by integration of technologies.
Proteome survey reveals modularity of the yeast cell machinery.
A global protein kinase and phosphatase interaction network in yeast.
Cell cycle arrest caused by CLN gene deficiency in Saccharomyces cerevisiae resembles START-I arrest and is independent of the mating-pheromone signalling pathway.
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Null mutations in CLN1, CLN2 and CLN3 together arrest cells in G1; the arrest point is Start and is independent of the mating-pheromone signalling pathway.
"Null mutations in three genes encoding cyclin-like proteins (CLN1, CLN2, and
CLN3) in Saccharomyces cerevisiae cause cell cycle arrest in G1 (cln arrest)"
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Cln function is specifically required to transit Start, not for later cell cycle stages; cells arrested in S phase still completed division after Cln depletion.
"These results are consistent with a specific CLN requirement for START transit"
Cyclin-specific docking motifs promote phosphorylation of yeast signaling proteins by G1/S Cdk complexes.
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Ste5 and Ste20 fragments are phosphorylated by Cln1- and Cln2-containing Cdk complexes but not by Cln3-, Clb5- or Clb2-Cdk, establishing a Cln1/2-specific substrate class reached through LP docking motifs.
"phosphorylation of the Ste5 and Ste20 fragments was observed only with Cln1 and Cln2, and not with Cln3, Clb5, or Clb2"
A family of cyclin homologs that control the G1 phase in yeast.
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CLN1 and CLN2 were isolated as dosage suppressors of a cdc28 temperature-sensitive mutation and encode closely related cyclin homologs.
"Two Saccharomyces cerevisiae genes were isolated based upon their
dosage-dependent rescue of a temperature-sensitive mutation of the gene CDC28"
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Cln1 and Cln2 are close paralogs within the cyclin family.
"CLN1 and
CLN2 encode closely related proteins that also share homology with cyclins."
An essential G1 function for cyclin-like proteins in yeast.
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Any one of CLN1, CLN2 or CLN3 is sufficient for proliferation; eliminating all three arrests the cell cycle regardless of cell type.
"Mutational elimination of the CLN1, CLN2, and DAF1/WHI1 products leads
to cell cycle arrest independent of cell type, while expression of any one of
the genes allows cell proliferation"
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Conditional expression of CLN1 confined the essential Cln requirement to G1 phase, and Cln function decays rapidly once synthesis stops.
"Using strains where CLN1 was expressed
conditionally, the essential function of Cln proteins was found to be limited to
the G1 phase"
Comparison of the Saccharomyces cerevisiae G1 cyclins: Cln3 may be an upstream activator of Cln1, Cln2 and other cyclins.
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Cln1 and Cln2 are far more abundant than Cln3 and carry much stronger associated histone H1 kinase activity.
"We find that Cln3 is a much rarer protein than Cln1 or Cln2 and has a
much weaker associated histone H1 kinase activity"
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Cln1 and Cln2, unlike Cln3, are cell cycle regulated and are down-regulated by pheromone-induced G1 arrest.
"Unlike Cln1 and Cln2, Cln3 is
not significantly cell cycle regulated, nor is it down-regulated by mating
pheromone-induced G1 arrest."
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Artificially expressed CLN1 activates Start less efficiently than CLN3, consistent with Cln3 acting upstream and Cln1 acting as a downstream/feedback cyclin.
"In similar experiments, CLN1 is less efficient than CLN3 at
activating Start."
A family of cyclin-like proteins that interact with the Pho85 cyclin-dependent kinase.